ACE2: Its potential role and regulation in severe acute respiratory syndrome and COVID‐19

Rezaei, Mitra; Ziai, Seyed Ali; Fakhri, Sajad; Pouriran, Ramin

doi:10.1002/jcp.30041

Cited by 35 publications

(28 citation statements)

References 157 publications

(268 reference statements)

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“…As the primary receptor for cellular entry of SARS-CoV-2, ACE2 is widely expressed in the lungs, heart, liver, kidneys, and intestines [ 50 , 51 ]. Proper equilibrium of ACE and ACE2 is critical for maintenance of the renin–angiotensin–aldosterone system (RAAS), in which both of these enzymes work together to regulate many physiological processes, including but not limited to blood pressure, electrolyte homeostasis, and inflammation responses [ 52 ].…”

Section: Molecular Basis Of Sars-cov-2 Infectionmentioning

confidence: 99%

Human Stem Cell Models of SARS-CoV-2 Infection in the Cardiovascular System

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Trask

Peeples

et al. 2021

Stem Cell Rev and Rep

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The virus responsible for coronavirus disease 2019 (COVID-19), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has infected over 190 million people to date, causing a global pandemic. SARS-CoV-2 relies on binding of its spike glycoprotein to angiotensin-converting enzyme 2 (ACE2) for infection. In addition to fever, cough, and shortness of breath, severe cases of SARS-CoV-2 infection may result in the rapid overproduction of pro-inflammatory cytokines. This overactive immune response is known as a cytokine storm, which leads to several serious clinical manifestations such as acute respiratory distress syndrome and myocardial injury. Cardiovascular disorders such as acute coronary syndrome (ACS) and heart failure not only enhance disease progression at the onset of infection, but also arise in hospitalized patients with COVID-19. Tissue-specific differentiated cells and organoids derived from human pluripotent stem cells (hPSCs) serve as an excellent model to address how SARS-CoV-2 damages the lungs and the heart. In this review, we summarize the molecular basis of SARS-CoV-2 infection and the current clinical perspectives of the bidirectional relationship between the cardiovascular system and viral progression. Furthermore, we also address the utility of hPSCs as a dynamic model for SARS-CoV-2 research and clinical translation. Graphical abstract

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Section: Molecular Basis Of Sars-cov-2 Infectionmentioning

confidence: 99%

Human Stem Cell Models of SARS-CoV-2 Infection in the Cardiovascular System

Ernzen

Trask

Peeples

et al. 2021

Stem Cell Rev and Rep

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“…As might be understood, ADAM17 plays a crucial role in ACE-2 shedding into sACE-2. The cleavage of membrane anchor occurs through ADAM17, and it underlies its occurrence in body fluid as the AT receptor upregulates ADAM17, resulting in an increase in sACE-2, resulting in a decrease in SARS-COV-2 entry as the virus will interact with the soluble form instead of interacting with mACE-2 and invade the cells [43]. In addition, it is worth highlighting that the cleavage of mACE-2 occurs in a region called juxtamembrane, and its retention on the cell membrane is regulated by the binding of calmodulin, and as the calmodulin is inhibited, the scACE-2 is increasingly released [44].…”

Section: Ace-2 and Ardsmentioning

confidence: 99%

Do Changes in ACE-2 Expression Affect SARS-CoV-2 Virulence and Related Complications: A Closer Look into Membrane-Bound and Soluble Forms

Yalcin

Sukumaran

Al-Ruweidi

et al. 2021

IJMS

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The SARS-CoV-2 virus utilizes angiotensin converting enzyme (ACE-2) for cell entry and infection. This enzyme has important functions in the renin-angiotensin aldosterone system to preserve cardiovascular function. In addition to the heart, it is expressed in many tissues including the lung, intestines, brain, and kidney, however, its functions in these organs are mostly unknown. ACE-2 has membrane-bound and soluble forms. Its expression levels are altered in disease states and by a variety of medications. Currently, it is not clear how altered ACE-2 levels influence ACE-2 virulence and relevant complications. In addition, membrane-bound and soluble forms are thought to have different effects. Most work on this topic in the literature is on the SARS-CoV virus that has a high genetic resemblance to SARS-Co-V-2 and also uses ACE-2 enzyme to enter the cell, but with much lower affinity. More recent studies on SARS-CoV-2 are mainly clinical studies aiming at relating the effect of medications that are thought to influence ACE-2 levels, with COVID-19 outcomes for patients under these medications. This review paper aims to summarize what is known about the relationship between ACE-2 levels and SARS-CoV/SARS-CoV-2 virulence under altered ACE-2 expression states.

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“…Only minimal percentages of monocytes/macrophages in the lung expressed ACE2 [ 64 ]. It presents the possibility of direct cellular infection (with no ACE2 engagement) or the existence of other receptors involved in SARS-CoV-2 entrances [ 65 , 66 ]. In general, the critical role of the renin–angiotensin system (RAS) has been indicated in various pathological and physiological processes.…”

Section: Sars-cov-2 Infectionmentioning

confidence: 99%

Targeting Multiple Signal Transduction Pathways of SARS-CoV-2: Approaches to COVID-19 Therapeutic Candidates

et al. 2021

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Due to the complicated pathogenic pathways of coronavirus disease 2019 (COVID-19), related medicinal therapies have remained a clinical challenge. COVID-19 highlights the urgent need to develop mechanistic pathogenic pathways and effective agents for preventing/treating future epidemics. As a result, the destructive pathways of COVID-19 are in the line with clinical symptoms induced by severe acute coronary syndrome (SARS), including lung failure and pneumonia. Accordingly, revealing the exact signaling pathways, including inflammation, oxidative stress, apoptosis, and autophagy, as well as relative representative mediators such as tumor necrosis factor-α (TNF-α), nuclear factor erythroid 2-related factor 2 (Nrf2), Bax/caspases, and Beclin/LC3, respectively, will pave the road for combating COVID-19. Prevailing host factors and multiple steps of SARS-CoV-2 attachment/entry, replication, and assembly/release would be hopeful strategies against COVID-19. This is a comprehensive review of the destructive signaling pathways and host–pathogen interaction of SARS-CoV-2, as well as related therapeutic targets and treatment strategies, including potential natural products-based candidates.

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ACE2: Its potential role and regulation in severe acute respiratory syndrome and COVID‐19

Cited by 35 publications

References 157 publications

Human Stem Cell Models of SARS-CoV-2 Infection in the Cardiovascular System

Human Stem Cell Models of SARS-CoV-2 Infection in the Cardiovascular System

Do Changes in ACE-2 Expression Affect SARS-CoV-2 Virulence and Related Complications: A Closer Look into Membrane-Bound and Soluble Forms

Targeting Multiple Signal Transduction Pathways of SARS-CoV-2: Approaches to COVID-19 Therapeutic Candidates

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